Galectin-1 expression in innervated and denervated skeletal muscle

Svensson, Anna; Tågerud, Sven

doi:10.2478/s11658-008-0039-0

Cited by 6 publications

(5 citation statements)

References 35 publications

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“…For example, decorin is associated with modified proliferation and differentiation of myogenic cells in x-linked muscular dystrophy [45] and reticulocalbin 1 expression is altered in dystrophic muscles [46]. Galectin 1 has been implicated in myoblast differentiation, skeletal muscle development and muscle regeneration [47,48]. Similarly, proteins such as serpin H1 (a.k.a.…”

Section: Molecular Pathology Of Skeletal Muscle Is Reversed By Treatm...mentioning

confidence: 99%

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy

Mutsaers

Wishart

Lamont

et al. 2011

Human Molecular Genetics

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Low levels of full-length survival motor neuron (SMN) protein cause the motor neuron disease, spinal muscular atrophy (SMA). Although motor neurons undoubtedly contribute directly to SMA pathogenesis, the role of muscle is less clear. We demonstrate significant disruption to the molecular composition of skeletal muscle in pre-symptomatic severe SMA mice, in the absence of any detectable degenerative changes in lower motor neurons and with a molecular profile distinct from that of denervated muscle. Functional cluster analysis of proteomic data and phospho-histone H2AX labelling of DNA damage revealed increased activity of cell death pathways in SMA muscle. Robust upregulation of voltage-dependent anion-selective channel protein 2 (Vdac2) and downregulation of parvalbumin in severe SMA mice was confirmed in a milder SMA mouse model and in human patient muscle biopsies. Molecular pathology of skeletal muscle was ameliorated in mice treated with the FDA-approved histone deacetylase inhibitor, suberoylanilide hydroxamic acid. We conclude that intrinsic pathology of skeletal muscle is an important and reversible event in SMA and also suggest that muscle proteins have the potential to act as novel biomarkers in SMA.

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Section: Molecular Pathology Of Skeletal Muscle Is Reversed By Treatm...mentioning

confidence: 99%

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy

Mutsaers

Wishart

Lamont

et al. 2011

Human Molecular Genetics

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show abstract

“…Galectin‐1 also lacks a signal peptide but is reported to be more abundant in plasma of T2DM patients, which contrasts with our findings. However, galectin‐1 is highly expressed in skeletal muscle and exposure of skeletal muscle to glucose increases galectin‐1 . Thus, the elevations in plasma galectin‐1 in T2DM patients may primarily arise from skeletal muscle rather than adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Label‐free profiling of white adipose tissue of rats exhibiting high or low levels of intrinsic exercise capacity

et al. 2015

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Divergent selection has created rat phenotypes of high- and low-capacity runners (HCR and LCR, respectively) that have differences in aerobic capacity and correlated traits such as adiposity. We analysed visceral adipose tissue of HCR and LCR using label-free HDMSE profiling. The running capacity of HCR was 9-fold greater than LCR. Proteome profiling encompassed 448 proteins and detected 30 significant (p <0.05; false discovery rate <10%, calculated using q-values) differences. Approximately half of the proteins analysed were of mitochondrial origin, but there were no significant differences in the abundance of proteins involved in aerobic metabolism. Instead, adipose tissue of LCR rats exhibited greater abundances of proteins associated with adipogenesis (e.g. cathepsin D), endoplasmic reticulum stress (e.g. 78 kDa glucose response protein) and inflammation (e.g. Ig gamma-2B chain C region). Whereas the abundance anti-oxidant enzymes such as superoxide dismutase [Cu-Zn] was greater in HCR tissue. Putative adipokines were also detected, in particular protein S100-B, was 431 % more abundant in LCR adipose tissue. These findings reveal low running capacity is associated with a pathological profile in visceral adipose tissue proteome despite no detectable differences in mitochondrial protein abundance.

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“…Similarly, denervation of rat skeletal muscles decreases the expression of semaphorin mRNA in extra‐ and peri‐synaptic regions of muscles 195 . Denervation of mouse and rat hindlimb and hemidiaphragm upregulates the expression of galectin‐1 in extra‐ and peri‐synaptic muscle regions 196 . Autonomic nerve fibers in bones release the neuropeptide VIP, which decreases transcription of the gene for interleukin‐6, which then enhances the action of osteogenic protein‐1 that, in turn, stimulates bone formation 197 .…”

Section: Neural Regulation Of Gene Expressionmentioning

confidence: 98%

“…195 Denervation of mouse and rat hindlimb and hemidiaphragm upregulates the expression of galectin-1 in extra-and peri-synaptic muscle regions. 196 Autonomic nerve fibers in bones release the neuropeptide VIP, which decreases transcription of the gene for interleukin-6, which then enhances the action of osteogenic protein-1 that, in turn, stimulates bone formation. 197 Destruction of the hypothalamic suprachiasmatic nucleus in rats abolishes the rhythms of Per gene expression and in mice leads to an arrhythmic circadian clock, but both adrenaline administration and electrical stimulation of the hepatic branch of the splanchnic nerve restores Per gene expression.…”

Section: Adjacent Neural Regulation Of Gene Expression In Peripheral ...mentioning

confidence: 99%

On the origin and nature of nongenetic information in eumetazoans

Cabej

2023

Annals of the New York Academy of Sciences

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Nongenetic information implies all the forms of biological information not related to genes and DNA in general. Despite the deep scientific relevance of the concept, we currently lack reliable knowledge about its carriers and origins; hence, we still do not understand its true nature. Given that genes are the targets of nongenetic information, it appears that a parsimonious approach to find the ultimate source of that information is to trace back the sequential steps of the causal chain upstream of the target genes up to the ultimate link as the source of the nongenetic information. From this perspective, I examine seven nongenetically determined phenomena: placement of locus‐specific epigenetic marks on DNA and histones, changes in snRNA expression patterns, neural induction of gene expression, site‐specific alternative gene splicing, predator‐induced morphological changes, and cultural inheritance. Based on the available evidence, I propose a general model of the common neural origin of all these forms of nongenetic information in eumetazoans.

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Galectin-1 expression in innervated and denervated skeletal muscle

Cited by 6 publications

References 35 publications

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy

Label‐free profiling of white adipose tissue of rats exhibiting high or low levels of intrinsic exercise capacity

On the origin and nature of nongenetic information in eumetazoans

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